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Molecular targets for therapy in systemic sclerosis

Iwamoto, Naoki; Distler, Oliver (2012). Molecular targets for therapy in systemic sclerosis. Fibrogenesis & Tissue Repair, 5(Suppl 1):S19.

Abstract

Despite significant advances have been made in the recent years regarding organ-specific therapies, there is no approved 'disease-modifying' antifibrotic drug for systemic sclerosis (SSc) available to date. Although non-selective immunosuppressive agents are routinely used to treat patients with SSc, large well-controlled studies are lacking for almost all immunosuppressive agents and further evidence is required for long-term beneficial effects of these drugs. Considering these facts about immunosuppressive agents in SSc and also considering the high mortality of SSc, other therapeutic strategies are urgently needed. Recently an important role of the 5-hydroxytryptamine (5-HT: serotonin) pathway in fibrosis was reported. In this review, we discuss the role of 5-HT in fibrosis and therapeutic potential of this molecule. Besides 5-HT, there are a number of promising targets that have been extensively characterized in recent years. For many of these molecular targets, modifiers are readily available for clinical studies, and often these modifiers are used already in clinical use for other diseases. Results from these studies will show, in how far the promising preclinical results for novel antifibrotic strategies can be translated to clinical practice.

Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Rheumatology Clinic and Institute of Physical Medicine
Dewey Decimal Classification:610 Medicine & health
Scopus Subject Areas:Health Sciences > Medicine (miscellaneous)
Health Sciences > Rheumatology
Health Sciences > Hepatology
Health Sciences > Dermatology
Health Sciences > Gastroenterology
Language:English
Date:2012
Deposited On:15 Feb 2013 07:42
Last Modified:25 Oct 2024 03:30
Publisher:BioMed Central
ISSN:1755-1536
OA Status:Hybrid
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:https://doi.org/10.1186/1755-1536-5-S1-S19
PubMed ID:23259845
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